Regulating the SV & HR Flashcards

1
Q

What is cardiac ischaemia?

A

A reduction in blood flow to the heart muscle. Usually due to constriction of coronary arteries

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2
Q

What does the hearts inotropic state refer to?

A

The strength of the muscles contraction

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3
Q

How does physiological increase of the HR work?

A

Sympathetic fibres release noradrenaline which works alongiside adrenaline circulating from the adrenal medulla.
Noradrenaline/Adrenaline work on B1-receptors in the sinoatrial node to increase the slope of the pacemaker potential and thus HR

(Also decrease in parasympathetic tone)

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4
Q

How does physiological decrease in HR work?

A

Parasympathetic fibres in the vagus nerve release acetylcholine.
ACh acts on muscarinic receptors in the sinoatrial node.
The Cell hyperpolarises and the slope of the pacemaker potential lengthens causing a decrease in HR

(Also decrease in sympathetic tone)

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5
Q

What 4 things affect Stroke Volume?

A

Preload
Afterload
Neural tone
Pathologys

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6
Q

What is preload?

A

the initial length of the muscle fibres

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7
Q

What is starlings law?

A

Starling’s law dictates that the initial length of the muscle (preload) is proportional to the energy of contraction

Meaning increasing preload will increase energy of contraction and thus SV

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8
Q

What determines preload?

A

The End Diastolic Volume because it stretches the muscle fibres

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9
Q

How does EDV relate to SV?

A

An increased EDV leads to an increased SV
A decreased EDV leads to a decreased SV

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10
Q

What determines EDV?

A

The venous return to that side of the heart

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11
Q

How is the stroke volume of each side kept equal?

A

The stroke volume of the right side is the amount of blood that returns to the left side through the pulmonary veins.
Since: venous return -> EDV -> preload -> SV the venous return to the left should be the same as that of the right.

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12
Q

What vessels can affect preload?

A

The capacitance vessels like venules and veins

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13
Q

What is afterload?

A

The load against which the muscle is trying to contract. In the left side of the heart this is the arterial pressure holding shut the aortic valve

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14
Q

What effects aortic pressure? and what does this mean for the SV?

A

The total peripheral resistance (TPR).
- TPR increase
->Ventricle requires more energy to force open the valve
-> Ventricle has less energy for ejecting blood
-> SV decreases.

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15
Q

How does the parasympathetic system affect SV?

A

Noradrenaline/Adrenaline act on B1-receptors in myocytes.
Contractility increases (inotropic effect)
A Shorter, Stronger contraction occurs
Increased SV

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16
Q

Why doesnt the parasympathetic system have much control over the SV?

A

Probably cos the Vagus nerve only innervates the sinoatrial nerve not the ventricular muscle itself.

17
Q

How does serum calcium affect Stroke Volume?

A

Hypercalcemia:
Ap fired -> more than normal calcium drawn into the cell -> more troponin is saturated -> More cross bridges acting -> greater strength of contraction
So shifts the EDV vs SV graph up and to the left

Hypocalcemia:
Lower strength of contraction. Opposite of above.
So shifts EDV vs SV graph down and to the right.

18
Q

What effect does cardiac ischaemia have on the SV vs EDV graph?

A

Shifts it down and to the right (i.e. reduces strength of contraction for any given EDV value)

19
Q

What happens to the heart when theres one sided ischaemia?

A

One side pumps more than the other
So the damaged side has a greater input then output meaning its EDV slowly increases

20
Q

How does the heart compensate for one sided ischaemia?

A

As EDV increases stroke volume increases.
Eventually it reaches a stage where stroke volume is back to normal so it stabilizes
This allows people to maintain a normal resting cardiac output despite ischaemia

21
Q

How do we tell if someone with a normal resting CO is ischaemic?

A

They’ll have reduced ejection fraction and capacity for exercise.

22
Q

What effect do barbiturates have on SV?

A

They decrease it, shifting the SV vs EDV graph down and to the right.

23
Q

Calculate CO?

A

CO = HR x SV

24
Q

An increase in HR should increase CO, why does it drop again above ~150bpm?

A

Increasing HR cuts into the filling time.
Above ~150bpm it starts to reduce the rapid filling phase, this is where it has a significant effect on EDV.
Since EDV -> Preload -> SV, stroke volume falls as EDV falls.

25
Q

What can cause an increase in heart rate that will lead to an increased CO?

A

An electric pacemaker
Increased Symp. Tone
Decreased Vagal Tone

26
Q

How does contractility of muscle affect CO?

A

Increasing contractility of muscle shortens systole and increases the CO.

27
Q

What can increase the contractility of muscle?

A

Increased Symp. Tone

28
Q

How does Venous return affect CO?

A

Increased Venous Return
-> EDV increases
-> Preload Increases
-> SV increases

(this offsets the reduced filling time caused by an increased HR to some extent and so somewhat maintains SV as HR increases)

29
Q

What causes increased venous return during exercise?

A

Venoconstriction
Blood pumped out of skeletal muscle by contraction
Blood pumped out of lungs by inhalation

30
Q

How does TPR increase CO during exercise?

A

During exercise arterioles dilate in skin, muscles & heart.
Therfore TPR decreases
Therefore Afterload decreases
Therefore SV & so CO increases.

31
Q

How much does CO increase during exercise?

A

4-6 times.